Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better activity, selectivity, and safety.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate Reaxense.
The library includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
Our top-notch dedicated system is used to design specialised libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes in-depth molecular simulations of both the catalytic and allosteric binding pockets, with ensemble virtual screening focusing on their conformational flexibility. For modulators, the process includes considering the structural shifts due to reaction intermediates to boost activity and selectivity.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
P00491
UPID:
PNPH_HUMAN
Alternative names:
Inosine phosphorylase; Inosine-guanosine phosphorylase
Alternative UPACC:
P00491; B2R8S5; D3DS00; Q15160; Q5PZ03
Background:
Purine nucleoside phosphorylase (PNP), also known as Inosine phosphorylase and Inosine-guanosine phosphorylase, plays a crucial role in the purine salvage pathway. It catalyzes the phosphorolytic breakdown of N-glycosidic bonds in beta-(deoxy)ribonucleoside molecules, leading to the formation of free purine bases and pentose-1-phosphate. This enzyme preferentially acts on 6-oxopurine nucleosides, including inosine and guanosine.
Therapeutic significance:
PNP deficiency disrupts the catabolism of inosine into hypoxanthine and guanosine into guanine, causing accumulation of guanosine and inosine. This leads to recurrent infections due to severe T-cell immunodeficiency and potential neurologic impairment. Understanding the role of PNP could open doors to potential therapeutic strategies for treating PNP deficiency.